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Andras Perl

Researcher at State University of New York Upstate Medical University

Publications -  208
Citations -  16848

Andras Perl is an academic researcher from State University of New York Upstate Medical University. The author has contributed to research in topics: Systemic lupus erythematosus & Lupus erythematosus. The author has an hindex of 59, co-authored 196 publications receiving 14134 citations. Previous affiliations of Andras Perl include Roswell Park Cancer Institute & State University of New York System.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
Journal ArticleDOI

Mitochondrial hyperpolarization and ATP depletion in patients with systemic lupus erythematosus.

TL;DR: T cell activation and apoptosis are mediated by deltapsim elevation and increased ROI production and Mitochondrial hyperpolarization and the resultant ATP depletion sensitize T cells for necrosis, which may significantly contribute to inflammation in patients with SLE.
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Rapamycin reduces disease activity and normalizes T cell activation–induced calcium fluxing in patients with systemic lupus erythematosus

TL;DR: Investigating whether rapamycin is beneficial in patients with SLE found mitochondrial dysfunction and Ca2+ fluxing could serve as biomarkers to guide decisions regarding future therapeutic interventions in SLE.